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Contribution of inflammatory processes to Alzheimer's disease: molecular mechanisms
Sastre M, Klockgether T, Heneka MT.. International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience, 2006-02-10
Topic: Amyloid, tau and blood-test diagnosis
There is compelling evidence that Alzheimer's disease (AD) amyloid-beta (Abeta) deposition is associated with a local inflammatory response, which is initiated by the activation of microglia and the recruitment of astrocytes. These cells secrete a number of cytokines and neurotoxic products that may contribute to neuronal degeneration and cell death. It has been documented that long-term intake of non-steroidal anti-inflammatory drugs (NSAIDs) decrease the risk for developing AD and delay the onset of the disease. The mechanism behind these NSAIDs is still controversial and several hypotheses have been raised, including changes in the amyloid precursor protein (APP) metabolism, in Abeta aggregation and a decrease in inflammatory mediators. Recently, it was proposed that some NSAIDs might activate the peroxisome proliferator-activated receptor-gamma (PPAR-gamma). PPAR-gamma belongs to a family of nuclear receptors that are able to regulate the transcription of pro-inflammatory molecules, such as iNOS. The activation of PPAR-gamma has been recently reported to reduce Abeta levels in cell culture and AD animal models. The implication of PPAR-gamma in the control of Abeta-induced inflammation suggests a new target for AD therapy and emphasize the contribution of neuroinflammatory mechanisms to the pathogenesis of AD.
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APA 7th
Sastre, M., Klockgether, T., & Heneka, M. T. (2006). Contribution of inflammatory processes to Alzheimer's disease: molecular mechanisms. International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience. https://doi.org/10.1016/j.ijdevneu.2005.11.014
Vancouver
Sastre M, Klockgether T, Heneka MT. Contribution of inflammatory processes to Alzheimer's disease: molecular mechanisms. International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience. 2006. doi:10.1016/j.ijdevneu.2005.11.014. PMID: 16472958.
BibTeX
@article{sastre2006-16472958,
author = {Sastre, M. and Klockgether, T. and Heneka, M. T.},
title = {{Contribution of inflammatory processes to Alzheimer's disease: molecular mechanisms}},
journal = {International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience},
year = {2006},
doi = {10.1016/j.ijdevneu.2005.11.014},
pmid = {16472958},
url = {https://doi.org/10.1016/j.ijdevneu.2005.11.014}
}
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Key findings
- There is compelling evidence that Alzheimer's disease (AD) amyloid-beta (Abeta) deposition is associated with a local inflammatory response, which is initiated by the activation of microglia and the recruitment of astrocytes.
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Study details
- Evidence strengthLow
How this study scored 36/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multi-centre collaboration, so those were left out: it earned 21 of the 58 points we could judge it on, which is 36 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2006 — older than 20 years, still counted |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 16472958) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 21 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 21 of the 58 points we could judge it on is 36 out of 100. |
| Total | 36 / 100 | — |
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